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Prenatal Death (prenatal + death)
Selected AbstractsPregnancy outcome in severe placental abruptionBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 7 2003Salma Imran Kayani Objective To determine the relationship between decision to delivery interval and perinatal outcome in severe placental abruption. Design A case,control study. Setting Large inner city teaching hospital. Methods Retrospective case note review of pregnancies terminated following severe placental aburption and fetal bradycardia. One year paediatric follow up by case note review or postal questionnaire. The differences in outcome (death or cerebral palsy) were examined using non-parametric and univariate analysis for the following time periods , times from onset of symptoms to delivery, onset of symptoms to admission, admission to delivery, onset bradycardia to delivery and decision to delivery interval. Main outcome measures Prenatal death or survival with cerebral palsy. Results Thirty-three women with singleton pregnancies over 28 weeks of gestation, admitted with clinically overt placental abruption, where delivery was effected for fetal bradycardia. Eleven of the pregnancies had a poor outcome (cases), eight infants died and three surviving infants have cerebral palsy. Twenty-two pregnancies had a good outcome (controls): survival with no developmental delay. No statistically significant relationship was found between maternal age, parity, gestation, or birthweight and a poor outcome. A statistically significant relationship between time from decision to delivery was identified (P= 0.02, Mann,Whitney U test). The results of a univariate logistic regression for this variable suggest that the odds ratio of a poor outcome for delivery at 20 minutes compared with 30 minutes is 0.44 (95% CI 0.22,0.86). Fifty-five percent of infants were delivered within 20 minutes of the decision to deliver. Serious maternal morbidity was rare. Conclusion In this small study of severe placental abruption complicated by fetal bradycardia, a decision to delivery interval of 20 minutes or less was associated with substantially reduced neonatal morbidity and mortality. [source] Neural precursor cells from a fatal human motoneuron disease differentiate despite aberrant gene expressionDEVELOPMENTAL NEUROBIOLOGY, Issue 3 2007Niklas Pakkasjärvi Abstract Precursor cells of the human central nervous system can be cultured in vitro to reveal pathogenesis of diseases or developmental disorders. Here, we have studied the biology of neural precursor cells (NPCs) from patients of lethal congenital contracture syndrome (LCCS), a severe motoneuron disease leading to prenatal death before the 32nd gestational week. LCCS fetuses are immobile because of a motoneuron defect, seen as degeneration of the anterior horn and descending tracts of the developing spinal cord. The genetic defect for the syndrome is unknown. We show that NPCs isolated postmortem from LCCS fetuses grow and are maintained in culture, but display increased cell cycle activity. Global transcript analysis of undifferentiated LCCS precursor cells present with changes in EGF-related signaling when compared with healthy age-matched human controls. Further, we show that LCCS-derived NPCs differentiate into cells of neuronal and glial lineage and that the initial differentiation is not accompanied by overt apoptosis. Cells expressing markers Islet-1 and Hb9 are also generated from the LCCS NPCs, suggesting that the pathogenic mechanism of LCCS does not directly affect the differentiation capacity or survival of the cells, but the absence of motoneurons in LCCS may be caused by a noncell autonomous mechanism. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007 [source] Uterine evaluation and gestation diagnosis in owl monkey (Aotus azarai infulatus) using the B mode ultrasoundJOURNAL OF MEDICAL PRIMATOLOGY, Issue 3 2006Frederico O B Monteiro Abstract Background, Gynecological and obstetrical ultrasonography has become an indispensable tool in the routine management, health evaluation and research on captive non-human primates. Methods, Ultrasound was used to evaluate the uterus and estimate the gestation of owl monkeys. Twelve couples were selected, where five were primiparous and seven multiparous females from the National Primate Center reproductive colony, Ananindeua-PA, Brazil. The procedures were carried out using the GE® Logiq 100 MP, equipped with a 7.5 MHz linear probe. Results, The females showed a simple uterus, of elongated shape, regular outline and homogeneous echogenic texture. In the uterine measurements craniocaudal diameter, dorsoventral diameter and uterine volume (UV), significant differences were identified (P < 0.05) between ultrasound examinations of primiparous and multiparous females. The UV showed a positive correlation with the number of births. The gestational sac and the embryonic echo were visible between 28 and 38 days after mating. Between 48 and 68 days after mating, embryonic death was identified in all the gestations. Conclusions, The chemical (use of tranquilizers) and husbandry factors (capture stress) may be related to the prenatal death. The establishing methods of conditioning the female to the ultrasonographic exam may offer a solution to this problem. [source] Expression of human tissue factor under the control of the mouse tissue factor promoter mediates normal hemostasis in knock-in miceJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2 2008L. A. SNYDER Summary.,Background:,Tissue factor (TF) is expressed widely at the subluminal surface of blood vessels and serves as the primary cellular initiator of the extrinsic pathway of blood coagulation. Lack of TF in mice resulted in lethality in utero, but human TF (huTF) expressed at low levels from a human minigene rescued null mice from prenatal death. Although these low-TF expressing transgenic mice developed to term, they had a significantly shorter life span and exhibited hemorrhage and fibrosis in the heart. Methods:,Human TF knock-in (TFKI) mice were generated by replacing the first two exons of the mouse (murine) TF (muTF) gene with the huTF complete coding sequence, thus placing it under the control of the endogenous muTF promoter. Results:,Expression of huTF in the TFKI mice was similar to muTF in wild-type (wt) mice. The TFKI mice showed no microscopic evidence of spontaneous hemorrhage in the heart, nor cardiac fibrosis at up to 18 months of age. Immunohistochemistry showed that huTF was expressed in cells surrounding blood vessels in TFKI mice. Coagulation activity of brain homogenates from TFKI mice was comparable with that from wt brain. Cardiac hemorrhage similar to that of the low-TF transgenic mice occurred in the TFKI mice when huTF was blocked by a neutralizing anti-huTF monoclonal antibody. Conclusion:,We generated a transgenic mouse line that expresses huTF under the control of the endogenous muTF promoter at physiological levels. Our results suggest that huTF can fully reconstitute the murine coagulation system and mediate normal hemostasis. [source] Prenatal ultrasound diagnosis of vasa praevia and analysis of risk factorsPRENATAL DIAGNOSIS, Issue 7 2007S. Baulies Abstract Objective To evaluate the role of ultrasound in prenatal diagnosis of vasa praevia (VP) and to asses the risk of VP associated with different causal factors. Material and Methods A retrospective study of the incidence of VP in a series of 12 063 deliveries between January 2000 and March 2005. We also studied the factors that predisposed for VP and the perinatal outcome of pregnancies. Results The prevalence of VP in our centre during this period was 0.07% (9 cases). All cases were prenatally diagnosed. The mean gestational age at diagnosis was 26 weeks. Multivariate analysis revealed the following associated factors: IVF pregnancies, bilobate or succenturiate placenta, and second-trimester placenta praevia, with an odds ratio of 7.75, 22.11 and 22.86, respectively. Conclusions In our series, the prenatal diagnosis of all cases of VP achieved during the second-trimester scan allowed us to avoid any prenatal death related to this condition. Copyright © 2007 John Wiley & Sons, Ltd. [source] |